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References 409

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Other Rare Causes

Pancreatic divisum

Pancreatic divisum (PD) is the most common congenital malformation of the pancreas. It involves a congenital disconnection between the main pancreatic duct and the major papilla. PD is classified as an obstructive cause of CP [3]. Although increased pressure in the dorsal pancreatic duct and minor papilla have been reported in PD, the majority of patients with PD are asymptomatic. Therefore, there is considerable debate as to whether it is causally associated with pancreatitis or abdominal pain [39]. Some reports indicate that the existence of a genetic cofactor plus PD leads to the development of CP. Garg et al. reported SPINK1 mutations in 41.7% of patients with PD and ICP, which was significantly higher than 2% in healthy controls. They also reported that 41.7% of patients carried CFTR gene polymorphisms [40]. Bertin et al. reported the frequency of PD in patients with RAP or CP is sign ificantly associated with CFTR mutations or polymorphisms [41].

Autoimmune Pancreatitis

Autoimmune pancreatitis (AIP) is a distinct form of pancreatitis. Therapeutically, AIP has a dramatic response to steroids. AIP is classified into type 1, which is a type of IgG4- related systemic disease, and type 2, which frequently accompanies inflammatory bowel disease [42]. Currently, the long- term prognosis of AIP is not well understood. However, an international study group reported pancreatic duct stones in 7% of patients with type 1 AIP, but not in patients with type 2 AIP [43]. According to a report from Japan, among 52 patients with type 1 AIP who had no pancreatic stones at diagnosis, 20 (38.5%) of them developed de novo pancreatic

stones after 3 or more years of follow- up [44]. The relationship between AIP and classic CP will become clearer in the future.

Hyperparathyroidism

The causal relationship between primary hyperparathyroidism (hypercalcemia) and RAP or CP is debatable. A systematic review demonstrated AP or CP occurred in

1.5% to 15.3% of patients with primary hyperparathyroidism, but the included studies had confounding factors, biases, and a lack of appropriate controls. In addition, the authors suggested the pancreatitis in this setting is likely the result of additional genetic and environmental factors [45]. Aslam etal. reported that hyperparathyroidism accounted for 1.94% of RAP or CP cases. In patients with CP associated with hyperparathyroidism, severe pain was a predominant symptom. After parathyroidectomy and subsequent decreases in serumcalcium levels, there was a reduction in their symptoms[46].

Hyperlipidemia

Hypertriglyceridemia is a well- established but underestimated cause of AP and RAP. However, whether hypertriglyceridemia can cause CP has not been well studied [47]. Vipperla etal. performed a retrospective study that reviewed the medical records of 121 patients with serum triglyceride levels of ≥500 mg/dL who experienced 225 attacks of AP between 2001 to 2013 at their institute in the United States. They found 20 (16.5%) of 121 patients were diagnosed with CP (9with preexisting CP, 11with new- onset CP during follow- up) [48]. Their relatively small single- center retrospective study needs to be validated in future prospective or large multicenter studies with simultaneous analysis of confounding factors such as alcohol intake and smoking.

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nationwide epidemiological survey for chronic pancreatitis in Japan: clinical significance of smoking habit in Japanese patients. Pancreatology 2014;14(6):490–496.

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Epidemiology of pancreatic disease in Lüneburg County. Astudy in a defined German population. Pancreatology 2002;2(5):469–477.

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Prevalence and clinical features of chronic pancreatitis in China: a retrospective multicenter analysis over 10 years. Pancreas 2009;38(3):248–254.

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pancreatitis: report from a multicenter Italian survey (PanCroInfAISP) on 893 patients. Dig Liver Dis 2009;41(4):311–317.

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the clinical onset of chronic pancreatitis and risk of pancreatic calcifications. Pancreas 2007;35(4):320–326.

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pancreatitis and progression to chronic pancreatitis after a first episode of acute pancreatitis. Clin Gastroenterol Hepatol 2016;14(5):738–746.

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risk of pancreatic calcification in late- onset but not early- onset idiopathic chronic pancreatitis. Pancreas 2000;21(2):115–119.

38 Zator Z, Whitcomb DC. Insights into the genetic risk

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management of pancreas divisum. Expert Rev Gastroenterol Hepatol 2019;13(11):1089–1105.

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SPINK1 gene mutation and CFTR gene polymorphisms in patients with pancreas divisum presenting with idiopathic pancreatitis. J Clin Gastroenterol 2009;43(9):848–852.

41 Bertin C, Pelletier AL, Vullierme MP etal. Pancreas

divisum is not a cause of pancreatitis by itself but act as a partner of genetic mutations. Am J Gastroenterol 2012;107(2):311–317.

42 Shimosegawa T, Chari ST, Frulloni L etal. International

consensus diagnostic criteria for autoimmune pancreatitis: guidelines of the International Association of Pancreatology. Pancreas 2011;40(3):352–358.

43 Hart PA, Kamisawa T, Brugge WR etal. Long- term

outcomes of autoimmune pancreatitis: a multicenter, international analysis. Gut 2013;62(12):1771–1776.

44 Maruyama M, Arakura N, Ozaki Y etal. Risk factors for

pancreatic stone formation in autoimmune pancreatitis over

term course. J Gastroenterol 2012;47(5):553–560.

a long-

45 Bai HX, Giefer M, Patel M, Orabi AI, Husain SZ. The

association of primary hyperparathyroidism with pancreatitis. J Clin Gastroenterol 2012;46(8):656–661.

46 Aslam M, Talukdar R, Jagtap M etal. Clinical profile and

outcome of parathyroid adenoma-

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Saudi J Med Med Sci 2018;6(2):95–99.

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hypertriglyceridemic pancreatitis: an update. J Clin Gastroenterol 2014;48(3):195–203.

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and natural course in a large cohort of patients with hypertriglyceridemia and pancreatitis. J Clin Gastroenterol 2017;51(1):77–85.

412

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Early Chronic Pancreatitis

Kazuhiro Kikuta and Atsushi Masamune

Division of Gastroenterology, Tohoku University Graduate School of Medicine, Miyagi, Japan

Concept/Definition

The concept of chronic pancreatitis was established by Comfort etal. in 1946[1,2]. They proposed that chronic pancreatitis was characterized by the progressive destruction of the pancreas. In the subsequently defined classification systems such as the Marseille classification [3], Cambridge classification [4], and MarseilleRoma classification [5], irreversible pancreatic changes associated with chronic pancreatitis were considered to cause permanent loss of pancreatic exocrine and endocrine functions. The conventional diagnostic criteria for chronic pancreatitis only enable us to detect the disease at the end stage, which ought to be irreversible. To improve the prognosis of chronic pancreatitis patients, it is indispensable to diagnose chronic pancreatitis in the early stage and prevent its progression through early interventions.

In 1996, the term “early- stage alcoholic chronic pancreatitis” was used to define a clinical stage linking alcoholic acute pancreatitis and alcoholic chronic pancreatitis by Ammann etal.[6]. They emphasized that the diagnosis “earlyfirmed by criteria independent from histology, i.e., the long- term follow- up that eventually revealed the typical clinical features of chronic pancreatitis. It could only be diagnosed in a retrospective manner.

The category of early chronic pancreatitis was the first to be introduced into the diagnostic criteria proposed by the Japan Pancreas Society in 2009 [7]. Early chronic pancreatitis corresponds to the stage at which chronic pancreatitis has already started with clinical symptoms and signs of pancreatic injury; however, characteristic morphological changes of the pancreas have still not been detected clearly on conventional imaging

stage alcoholic chronic pancreatitis” was con-

modalities. Theoretically early chronic pancreatitis is considered to be a reversible pathological condition[8].

A new mechanistic definition of chronic pancreatitis was proposed by Whitcomb etal. in 2016[9]. A conceptual model of chronic pancreatitis was derived, recognizing that subjects may exist in: (A) “at- risk” state of chronic pancreatitis, or in four active states; (B) acute pancreatitis recurrent acute pancreatitis; (C) early chronic pancreatitis; (D) established chronic pancreatitis; and (E) end- stage chronic pancreatitis (Fig.50.1). Early chronic pancreatitis may overlap conceptually with “minimal change chronic pancreatitis” or “pre- chronic pancreatitis,” depending on eventual diagnostic criteria and distinctions from other states. The transition from “B” to “C” involves detection of biomarkers of chronic pancreatitis pathogenesis or pathology, but does not reach a state of “D.” Biomarkers may be biochemical, structural or functional. The transition from “C” to “D” involves progression of disease to a persistent state of pathology or dysfunction. This new definition of chronic pancreatitis may allow for a rational approach to early diagnosis.

However, there still has not been international consensus on the definition of early chronic pancreatitis. In 2018, international consensus statements on early chronic pancreatitis were developed by a working group for the international consensus guidelines for chronic pancreatitis in collaboration with the International Association of Pancreatology, American Pancreatic Association, Japan Pancreas Society, PancreasFest Working Group, and European Pancreatic Club [10]: morphology- based diagnosis of early chronic pancreatitis is not possible without additional information; new approaches to the accurate diagnosis of early chronic pancreatitis will require a mechanistic definition; such a definition will require prospective validation.

The Pancreas: An Integrated Textbook of Basic Science, Medicine, and Surgery, Fourth Edition. Edited by Hans G. Beger, Markus W. Büchler, RalphH. Hruban, Julia Mayerle, John P. Neoptolemos, Tooru Shimosegawa, Andrew L. Warshaw, David C. Whitcomb, and Yupei Zhao. © 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd. Companion website: www.wiley.com/go/beger/thepancreas4e

Diagnosis 413

A. “At Risk”

B. “AP-RAP”

C. “Early CP”

D. “Established CP” E. “End-Stage CP”

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Injury

Susceptibility

factors

(asymptomatic)

Years Days Months Months to years Remainder of life

Figure50.1 A conceptual model of chronic pancreatitis used for definition development[9]. AP: acute pancreatitis; RAP: recurrent acute

pancreatitis; CP: chronic pancreatitis; SAPE: sentinel acute pancreatitis event; DM: diabetes mellitus; PDAC: pancreatic ductal adenocarcinoma. Source: Whitcomb etal. 2016[9]. With permission of Elsevier.

SAPE,

then RAP

Susceptibility to

recurrence

biomarkers

Resolve

Risk Factors/Etiology

Injury or

stress

Immune dysregulation

Acinar dysfunction

Islet dysfunction

Pathologic pain

Metaplasia

Therapeutic approaches

Progression

pathways

Fibrosis/sclerosis

Exocrine insufficiency

DM(T3c)

Pain Syndrome

PDAC

Symptomatic and

supportive treatment

pancreatitis [9,10,14,15]. However, some patients with chronic pancreatitis are asymptomatic during the early

Based on the new mechanistic definition of chronic pancreatitis[9], the risk factors of early chronic pancreatitis can be considered similar to those of recurrent acute pancreatitis and chronic pancreatitis. International classification systems such as TIGAR- O [11] and the M- ANNHEIM classification system [12] incorporate common etiological risks including alcohol and nicotine consumption, genetic mutations and polymorphisms,

stage, and incidental imaging findings, steatorrhea, or diabetes may be the first clinical manifestation of chronic pancreatitis. According to a nationwide epidemiological survey conducted in Japan, 91.4% of patients with early chronic pancreatitis had recurrent upper abdominal pain, and 81.5% had abnormal pancreatic enzyme levels in the serum or urine. Only 13.9% were positive for abnormal pancreatic exocrine function[13].

metabolic disorders, ductal obstruction, immunological factors, and idiopathic pancreatitis.

Diagnosis

Epidemiology

A nationwide epidemiological survey of early chronic pancreatitis was conducted in Japan [13]. Patients with early chronic pancreatitis who were diagnosed according to the Japanese diagnostic criteria 2009 [7] and had visited the selected hospitals in 2011 were surveyed. The estimated prevalence and the annual incidence of early chronic pancreatitis were 4.2 and 1.0 per 100,000 persons, respectively. The male- to- female sex ratio was 1.32 : 1. The mean age was

60.4 and the mean age at disease onset was 55.4. The common etiologies were idiopathic (47.7%) and alcoholic (45.0%).

Clinical Presentation

A history of acute pancreatitis, especially recurrent acute pancreatitis, is a significant risk factor for early chronic

There still has not been international consensus on the diagnostic criteria for early chronic pancreatitis.

In 2009, the Japan Pancreas Society proposed the world’s first diagnostic criteria for early chronic pancreatitis in the Japanese clinical diagnostic criteria for chronic pancreatitis 2009 (DC2009) [7]. In 2019, the Japan Pancreas Society proposed the revised DC2009, namely, “clinical diagnostic criteria for chronic pancreatitis 2019 (DC2019)” (Table50.1)[17]. Early chronic pancreatitis is diagnosed using a combination of five clinical signs: (i) repeated upper abdominal or back pain; (ii) abnormal pancreatic enzyme levels in the serum or urine; (iii) abnormal pancreatic exocrine function; (iv) continuous heavy drinking of alcohol equivalent to or more than 60 g/day of pure ethanol or mutation in the pancreatitisassociated gene such as PRSS1 and SPINK1; (v) past history of acute pancreatitis; and imaging findings on EUS, MRCP, or ERCP. Imaging findings on EUS were

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Table50.1 Japanese clinical diagnostic criteria for chronic

pancreatitis 2019 Source: [16]/Springer Nature.

Diagnostic items for chronic pancreatitis

① Characteristic imaging findings ② Characteristic histological findings ③ Repeated upper abdominal or back pain ④ Abnormal pancreatic enzyme levels in the serum or urine ⑤ Abnormal pancreatic exocrine function ⑥

Continuous heavy drinking of alcohol equivalent to ≧60 g/ day of pure ethanol or mutation in the pancreatitisassociated gene

⑦ Past history of acute pancreatitis

Imaging findings of early chronic pancreatitis Either (a) or (b)

a) More than two features among the following four EUS

findings including (1) or (2)

1) Hyperechoic foci (non- shadowing) or strands

2) Lobularity

3) Hyperechoic MPD margin

4) Dilated side branches

b) Irregular dilatation of more than three side branches on

MRCP or ERCP

Definite chronic pancreatitis: either (a) or (b)

a) Definite findings of ① or ② b) Probable findings of ① or ②, plus more than two items

among ③, ④, and ⑤

Probable chronic pancreatitis Probable findings of ① or ② Early chronic pancreatitis More than three items among ③~⑦ plus imaging findings of

early chronic pancreatitis

Note 1: Differential diagnosis from other pancreatic diseases especially pancreatic cancer and intraductal papillary mucinous neoplasm is important. Note 2: If imaging findings of early chronic pancreatitis were absent, a diagnosis of possible chronic pancreatitis could be made in the patients without ① and ②, but with more than three items among ③~⑦ after ruling out other diseases. Imaging examinations including EUS are recommended for the patients with possible chronic pancreatitis. Note 3: Patients with only two items among ③~⑦ and imaging findings of early chronic pancreatitis are regarded as possible early chronic pancreatitis after ruling out other diseases, and require careful follow- up. Footnote: Long- term prognosis should be clarified in patients with early chronic pancreatitis.

It has also been reported that three or more attacks of acute pancreatitis with no morphological changes to the pancreas can be an improved diagnostic criterion for early chronic pancreatitis[16].

Diagnostic Modalities forEarly Chronic Pancreatitis

Transabdominal Ultrasonography (US)

Transabdominal US is recommended as the first- line noninvasive imaging approach for evaluating patients with suspected chronic pancreatitis. However, the ability of transabdominal US to diagnose early chronic pancreatitis has not been fully validated. HaPanEU/UEG working group indicated that abdominal US can only be used to diagnose chronic pancreatitis at an advanced stage[17].

Computed Tomography (CT)

The ability of CT to diagnose early chronic pancreatitis has not been fully validated as well as transabdominal US.

Magnetic Resonance Imaging (MRI)

Japanese clinical diagnostic criteria for chronic pancreatitis 2019incorporated a finding of irregular dilation of more than three side branches on MRCP into diagnostic criteria for early chronic pancreatitis [16]. This MRCP finding has been defined in accordance with image grading “mild” of ERP defined in the Cambridge classification[4]. The ability of MRCP to diagnose early chronic pancreatitis needs to be prospectively verified.

T1- weighted MR signal of the pancreas, which was associated with pancreatic exocrine dysfunction[18] and the grade of ductal changes under the Cambridge classification [19], may be helpful in the evaluation of suspected early chronic pancreatitis. Main pancreatic duct irregularity, T1- weighted MR signal, and duodenal filling after secretin injection may be predictors of pancreatic fibrosis[20].

consolidated from seven items in DC2009 to four items: hyperechoic foci (non- shadowing) or strands; lobularity; hyperechoic MPD margin; dilated side branches. Early chronic pancreatitis can be diagnosed if a patient does not justify a diagnosis of definite or probable chronic pancreatitis, but satisfies at least three of five clinical signs and imaging findings of early chronic pancreatitis. The approach by the Japan Pancreas Society still has not been fully accepted internationally, while it provides a potentially useful definition of early chronic pancreatitis.

Endoscopic Ultrasonography (EUS)

EUS is considered the most sensitive modality for detecting early chronic pancreatitis, although early chronic pancreatitis may not be diagnosed by current imaging techniques [10]. So far, there is no consensus cutoff of EUS findings for establishing a diagnosis of early chronic pancreatitis.

In 2009, Japanese clinical diagnostic criteria incorporated EUS findings into diagnostic criteria for early chronic pancreatitis[7]. Considering the diagnosis of

Management/Treatment 415

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indeterminate for chronic pancreatitis based on the Rosemont classification [21], five features of pancreatic parenchymal factors (lobularity with honeycombing; lobularity without honeycombing; hyperechoic foci without shadowing; stranding; cysts) and two features of pancreatic ductal factors (dilated side branches; hyperechoic MPD margin) were adopted for the EUS findings of early chronic pancreatitis. In the 2019 revision of diagnostic criteria, EUS findings were consolidated from seven items to four items: lobularities with and without honeycombing were consolidated to lobularity; hyperechoic foci without shadowing and stranding were consolidated to hyperechoic foci (nonshadowing) or strands; and cysts were removed from the diagnostic items (Table 50.1) [16]. The interobserver reliability of EUS criteria of diagnostic criteria 2019 was higher than that of diagnostic criteria 2009[22].

Elastography

EUS- elastography has recently allowed the evaluation of the elasticity of deep organs, such as the pancreas[23,24]. The usefulness of EUS- elastography for the diagnosis of early chronic pancreatitis has yet to be established[25], although there has been a single arm study that patients with suspected early chronic pancreatitis had an abnormally high strain ratio at EUS- elastography[26].

tests for pancreatic insufficiency. The positive predictive value of the secretin pancreatic function testing for the subsequent development of chronic pancreatitis has been reported to be 45% with a negative predictive value of 97%[27].

The Japanese clinical diagnostic criteria incorporated a finding of abnormal results in BT- PABA test into diagnostic criteria for early chronic pancreatitis [7,16]. Based on this criteria, only 13.9% of early chronic pancreatitis was positive for abnormal pancreatic exocrine function[13].

Fecal elastase- 1 is considered to be inappropriate for the diagnosis of early chronic pancreatitis because the correlation of fetal elastase- 1with mild ductal changes is not strong[28,29].

Histological Evaluation

While conventional chronic pancreatitis has been diagnosed mainly on the basis of structural changes related to fibrosis, histological findings for the diagnosis of early chronic pancreatitis have not yet been established.

Furthermore, direct acquisition of pancreatic tissue for the diagnosis of early chronic pancreatitis is limited. It has been reported that EUS- guided fine- needle biopsy provided inadequate material for the histological diagnosis of early chronic pancreatitis[30].

ERCP

The Japanese clinical diagnostic criteria incorporated a finding of irregular dilation of more than three side branches on ERP into diagnostic criteria for early chronic pancreatitis[7,16]. This ERP finding has been defined in accordance with image grading “mild” defined in the Cambridge classification[4]. The ability of ERP to diagnose early chronic pancreatitis needs to be prospectively verified.

Pancreatic Function Testing

Exocrine pancreatic insufficiency is a common complication of chronic pancreatitis. Conversely, early chronic pancreatitis is considered to be a stage of chronic pancreatitis with preserved pancreatic function and potentially reversible features[10]. The usefulness of pancreatic function testing for the diagnosis of early chronic pancreatitis still has not been established, although it is considered that early chronic pancreatitis can be diagnosed by a combination of factors including pancreatic function testing[10].

Direct hormone- stimulated tests, using cholecystokinin

or secretin, are considered the most sensitive and specific

Biomarkers

So far, there are no widely accepted biomarkers for the diagnosis of early chronic pancreatitis [10]. There is a report that indicated the usefulness of blood- based microRNA biomarker panel for the diagnosis of early chronic pancreatitis[31].

Genetic Markers

Genetic variants are important risk factors for early chronic pancreatitis and can add specificity to the likely etiology, but they are neither necessary nor sufficient to make a diagnosis of early chronic pancreatitis[10]. The Japanese clinical diagnostic criteria has incorporated mutations in the pancreatitis- associated genes such as PRSS1 and SPINK1 for the diagnosis of early chronic pancreatitis[16].

Management/Treatment

Evidence for the management of early chronic pancreatitis is insufficient.

In patients with acute pancreatitis or recurrent acute pancreatitis, it is important to evaluate risk factors in

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order to prevent disease progression[11]. It is expected that precision medicine will be established according to risk factors in the future. Alcohol abstinence and smoking cessation can be the mainstays for preventing the progression of early chronic pancreatitis.

It has been reported that a combination treatment of proton pump inhibitor, camostat mesilate, and pancrelipase improved epigastric pain[32] and EUS findings[33] in patients with early chronic pancreatitis.

References

1 Comfort MW, Gambill EE, Baggenstoss AH. Chronic

relapsing pancreatitis. A study of twentywithout associated disease of the biliary or gastrointestinal tract. Gastroenterology 1946;6:239–285.

2 Comfort MW, Gambill EE, Baggenstoss AH. Chronic

relapsing pancreatitis. A study of twentywithout associated disease of the biliary or gastrointestinal tract. Gastroenterology 1946;6:376–408.

3 Sarles H. Pancreatitis. Symposium of Marseille 1963.

Basel: Karger, 1965.

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Chronic Pancreatitis withInflammatory Mass inthe Pancreatic Head

Ulrich F. Wellner, Kim C. Honselmann, and Tobias Keck

Department of Surgery, University Medical Center Schleswig-Holstein, Campus Lübeck, Lübeck, Germany

Definition

Chronic pancreatitis can present with enlargement and mass- formation of the pancreatic head, mimicking virtually all symptoms of a malignant pancreatic head tumor and confronting the clinician with significant diagnostic and therapeutic challenges. This phenomenon has been termed the “inflammatory (pseudo) tumor”[1], “tumorforming chronic pancreatitis”[2], and other. For the purpose of this article, we will use the term inflammatory pancreatic head mass (IPHM).

From a pathophysiological point of view, IPHM is thought to result from recurrent acute and chronic inflammation of the pancreatic parenchyma, but at the same time to perpetuate disease progression as a “pacemaker” by causing main pancreatic duct (MPD) obstruction leading to chronic ductal hypertension[3]. There is no generally accepted definition of IPHM, but the following criteria may be applied: presence of an abnormally enlarged pancreatic head, often accompanied by pancreatic calcifications, MPD dilatation, and irregularities and atrophy of the pancreatic parenchyma to the left of the mesentericoportal axis[4–6] (Figs51.1 and51.2).

Incidence

The concept of the IPHM as a pacemaker of chronic pancreatitis has been established by Beger etal.[3] and followed mainly by European surgeons. The incidence of IPHM in surgical patients is in the range of 85%; however, exact figures have rarely been reported in detail[5,7]. The average size of the pancreatic head has been shown to be significantly larger in a study comparing German (median 4.5 cm) and North American (median 2.6 cm) patients undergoing surgery for chronic

pancreatitis [5]. The significance of this finding lies in the fact that it explains regional differences in operative procedures used to treat chronic pancreatitis; however, the underlying cause is not clear. Reasons might be a pattern of clinical transfer of the patient from the gastroenterologist to the surgeon, genetic differences, or different risk factors for the development of chronic pancreatitis.

Symptoms, Pathophysiology, and Clinical Problems

An IPHM can cause many clinical symptoms and complications, which in principle constitute the classical complications of chronic pancreatitis. Differential diagnosis and decision- making may be complicated as virtually all of these symptoms can also be caused by pancreatic head cancer.

One of the most frequently reported symptoms is pain[4,7]. Typically, the pain maximum is located to the epigastric area and may radiate to the flanks and back. In some cases, however, back pain may be the primary complaint. The pain can be episodic or continuous, with sudden exacerbations of variable frequency from daily to once in several months, often triggered by alcohol or food intake. Signs of acute pancreatitis like elevation of serum amylase or lipase and edematous swelling of the pancreatic head are often found associated with severe acute pain attacks, but may as well be missing, especially with longer duration of disease. In line with this, there is good evidence from histopathological and experimental studies that pancreatic pain is not only caused by acute inflammation but also from chronic neuropathy of visceral nerves in the pancreas [8]. Importantly about 50–90% of patients will not become pain10years after disease onset[9].

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